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A class of enzymes that remove acetyl groups from N6-acetyl-lysine residues on a histone. The reaction of this enzyme is opposite to that of EC 18.104.22.168, histone acetyltransferase. Histone deacetylases (HDACs) can be organized into three classes, HDAC1, HDAC2 and HDAC3, depending on sequence similarity and domain organization. Histone acetylation plays an important role in regulation of gene expression. In eukaryotes, HDACs play a key role in the regulation of transcription and cell proliferation . May be identical to EC 22.214.171.124, acyl-lysine deacylase.
nitrative/oxidative stress reduce HDAC2 expression via nitration of distinct tyrosine residues. Peroxynitrite, hydrogen peroxide and cigarette smoke-conditioned medium reduce HDAC2 expression in A549 epithelial cells in vitro. This reduction is due to increased proteasomal degradation following ubiquitination rather than reduction of mRNA expression or stability
down-regulation of HDAC gene HDA710 induces a semi-dwarf phenotype, down-regulation of HDAC gene HDA704 affects plant height and flag leaf development; down-regulation of HDAC gene HDA710 induces a semi-dwarf phenotype, down-regulation of HDAC gene HDA704 affects plant height and flag leaf development; down-regulation of HDAC gene HDA710 induces a semi-dwarf phenotype, down-regulation of HDAC gene HDA704 affects plant height and flag leaf development
knockdown of HDAC10 significantly increases the mRNA expression levels of thioredoxin-interacting protein and induces release of cytochrome c and activated apoptotic signaling molecules through accumulation of reactive oxygen species in SNU-620 human gastric cancer cells
HDAC inhibition improves DELTAF508 cystic fibrosis transmembrane conductance regulator stability and trafficking, silencing of HDAC2 and HDAC3 causes a 2.5fold and 1.5fold increase in DELTAF508 cystic fibrosis transmembrane conductance regulator mRNA, respectively, as well as an about 5fold increase in total DELTAF508 protein. Silencing of HDAC1 induces a 1.4fold stimulation of iodide efflux. In contrast, silencing of HDAC7 exhibits a 3.6fold stimulation of cAMP-mediated iodide efflux comparable to 30°C efflux
while brain development and adult stem cell fate are normal upon conditional deletion of HDAC2 or in mice lacking the catalytic activity of HDAC2, neurons derived from both zones of adult neurogenesis die at a specific maturation stage
inhibition of SIRT1 activity leads to a recovery from the intrinsic repressive activity of orphan nuclear receptor small heterodimer partner (SHP) but not of DAX1. Inhibition of SIRT1 significantly diminishes the repressive effect of SHP on liver receptor homolog 1 transactivity. Inhibition of SIRT1 activity significantly reverses SHP-mediated inhibition of bile-acid synthesis by liver receptor homolog 1 overexpression
depleting maternal isozyme HDAC2 results in hyperacetylation of H4K16, while normal deacetylation of other lysine residues of histone H3 or H4 is observed, and defective chromosome condensation and segregation during oocyte maturation occurs in a subpopulation of oocytes, leading to increased incidence of aneuploidy likely accounts for the observed sub-fertility of mice harboring Hdac2-defective oocytes. The infertility of mice harboring Hdac1-/+/Hdac2-/- oocytes is attributed to failure of those few eggs that properly mature to metaphase II to initiate DNA replication following fertilization. Hdac1-/+/Hdac2-/- eggs are fertilized but fail to initiate DNA replication. The increased amount of acetylated H4K16 likely impairs kinetochore function in oocytes lacking isozyme HDAC2 because kinetochores in mutant oocytes are less able to form coldstable microtubule attachments and less CENP-A is located at the c